<<Disclaimer: Verify this information before applying it to your situation.>> Celiac disease, IBS, Crohn's disease, hypochlorhydria (low stomach acid), as well as antibiotic use, can all disturb the mix of gut microflora. This can be a significant factor in the development of food allergies. A new study lends further support to the importance of maintaining a healthy mix of gut flora to ward-off food allergies. Toll-like receptors (TLR), located on the surface dendritic cells, epithelial cells and other immune system cells, sense structural components found only on the surface of bacteria and other pathogens. They are important as to how the immune system responds to microflora inhabiting the gut. There are at least 10 types of Toll-like receptors in humans (recently an 11th was identified) which identify specific kinds of bacterial components. The following study now has found an association between TLR4 and food allergies. TLR4 primarily senses lipopolysaccharides (LPS) found in the outer membrane of Gram-negative bacteria which can provoke immune responses, inflammation and have an endotoxic effect. The study finds that a disturbance of normal microflora, such as by antibiotics, increases allergic responses. Restoration of normal microflora reduces allergic responses. TLR4 signals provided by normal microflora may be a factor in reducing food allergies. ---------- J Immunol. 2004 Jun 1;172(11):6978-87 Toll-like receptor 4 signaling by intestinal microbes influences susceptibility to food allergy. Bashir ME, Louie S, Shi HN, Nagler-Anderson C. Mucosal Immunology Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129. The mechanisms by which signaling by the innate immune system controls susceptibility to allergy are poorly understood. In this report, we show that intragastric administration of a food allergen with a mucosal adjuvant induces allergen-specific IgE, elevated plasma histamine levels, and anaphylactic symptoms in three different strains of mice lacking a functional receptor for bacterial LPS (Toll-like receptor 4 (TLR4)), but not in MHC-matched or congenic controls. Susceptibility to allergy correlates with a Th2-biased cytokine response in both the mucosal (mesenteric lymph node and Peyer's patch) and systemic (spleen) tissues of TLR4-mutant or -deficient mice. TLR4-mutant mice are not inherently impaired in their ability to regulate Th1 cytokine production because they respond to stimulation via TLR9. Coadministration of CpG oligodeoxynucleotides during sensitization of TLR4-mutant mice with allergen plus CT abrogates anaphylactic symptoms and Ag-specific IgE, and results in a Th1-polarized cytokine response. When the composition of the bacterial flora is reduced and altered by antibiotic administration (beginning at 2 wk of age), TLR4 wild-type mice become as susceptible to the induction of allergy as their TLR4-mutant counterparts. Both allergen- specific IgE and Th2 cytokine responses are reduced in antibiotic-treated mice in which the flora has been allowed to repopulate. Taken together, our results suggest that TLR4-dependent signals provided by the intestinal commensal flora inhibit the development of allergic responses to food Ags. PMID: 15153518 [PubMed - in process] * * * *Support summarization of posts, reply to the SENDER not the Celiac List*